Global transcriptional profiling in porcine mammary glands from late pregnancy to peak lactation.
ABSTRACT Sow milk yield and quality is crucial for the survival and growth of piglets. To understand the molecular mechanisms of lactogenesis and lactation, mammary tissue samples were taken from six sows at -17(±2), 1 and 17(±2) days relative to parturition. Mammary tissues from two sows in the same stage were used to extract RNA, which were subsequently pooled in equal amounts. Nine pooled samples were hybridized to porcine Affymetrix GeneChips. Totally 1,524 genes were detected as significantly differentially expressed over the time course tested (p<0.01, q<0.01, fold change≥2 or ≤-2), including 709 upregulated and 575 downregulated genes identified at peak lactation compared to late pregnancy. Gene ontology analysis revealed that most of the upregulated genes were involved in transport, biosynthetic processes, and homeostasis, whereas most of the downregulated genes were involved in intracellular signaling cascades, cell cycle, and DNA replication. Furthermore, we identified 64 differentially expressed genes of the solute carrier families. Taken together, our microarray analysis provides insights into previously uncharacterized changes in transcriptome between late pregnancy and peak lactation in the porcine mammary gland. The solute carrier genes and other differentially expressed genes identified in this study will guide further characterization of their function to enhance milk yield and piglet growth.
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ABSTRACT: While aspects of cellular fatty acid uptake have been studied as early as 50 years ago, recent developments in this rapidly evolving field have yielded new functional insights on the individual mechanistic steps in this process. The extremely low aqueous solubility of long chain fatty acids (LCFA) together with the very high affinity of serum albumin and cytoplasmic fatty acid binding proteins for LCFA have challenged the limits of technology in resolving the individual steps of this process. To date no single mechanism alone accounts for regulation of cellular LCFA uptake. Key regulatory points in cellular uptake of LCFA include: the aqueous solubility of the LCFA; the driving force(s) for LCFA entry into the cell membrane; the relative roles of diffusional and protein mediated LCFA translocation across the plasma membrane; cytoplasmic LCFA binding protein-mediated uptake and/or intracellular diffusion; the activity of LCFA-CoA synthetase; and cytoplasmic protein mediated targeting of LCFA or LCFA-CoAs toward specific metabolic pathways. The emerging picture is that the cell has multiple, overlapping mechanisms that assure adequate uptake and directed intracellular movement of LCFA required for maintenance of physiological functions. The upcoming challenge is to take advantage of new advances in this field to elucidate the differential interactions between these pathways in intact cells and in tissues.The Journal of Lipid Research 09/1999; 40(8):1371-83. · 4.39 Impact Factor
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ABSTRACT: Thirty-two gilts were used to evaluate the effects of increased dietary energy and CP during late gestation on mammary development. On d 75 of gestation, gilts were assigned randomly in a 2 x 2 factorial arrangement to adequate (5.76 Mcal ME/d) or increased (10.5 Mcal ME/d) energy and adequate (216 g CP/d) or increased (330 g CP/d) protein. On d 105 of gestation, gilts were slaughtered and total mastectomies were performed. Mammary tissue was separated into mammary parenchymal and mammary extraparenchymal stromal tissue and analyzed for DNA, RNA, protein and lipid. No interactions between dietary energy and protein level were detected (P greater than .20). When adjusted for number of mammary glands and maternal BW (weight of the sow less the weight of the fetuses), mammary parenchymal weight was 27% greater (P less than .03) in gilts fed adequate energy than in gilts fed increased energy, but mammary extraparenchymal stroma weight was unaffected by dietary energy level. Total mammary parenchymal DNA was 30% greater in gilts fed adequate energy than in gilts fed increased energy (P less than .03). Total mammary parenchymal RNA (P less than .02) and total mammary parenchymal protein (P less than .02) also were greater in gilts fed adequate energy than in gilts fed increased energy. Dietary protein level did not affect mammary variables measured, except that increased dietary protein tended to reduce mammary extraparenchymal stromal weight (P less than .09). Increased dietary protein between d 75 and d 105 of gestation did not benefit mammary development, but increased dietary energy was detrimental to development of mammary secretory tissue.Journal of Animal Science 02/1991; 69(1):194-200. · 2.09 Impact Factor
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ABSTRACT: The mammary gland of the lactating mouse synthesizes and secretes milk lipid equivalent to its entire body weight in a single 20-day lactation cycle, making it one of the most active lipid synthetic organs known. We test the hypothesis that multiple control points and potential regulatory mechanisms regulate milk lipid synthesis at the level of gene expression. The mammary transcriptome of 130 genes involved in glucose metabolism was examined at late pregnancy and early lactation, utilizing data obtained from microarray analysis of mammary glands from quadruplicate FVB mice at pregnancy day 17 and lactation day 2. To correlate changes with physiological parameters, the metabolome obtained from magnetic resonance spectroscopy of flash-frozen glands at day 17 of pregnancy was compared with that at day 2 of lactation. A significant increase in carbohydrates (glucose, lactose, sialic acid) and amino acids (alanine, aspartate, arginine, glutamate) with a moderate increase in important osmolytes (myo-inositol, betaine, choline derivatives) were observed in the lactating gland. In addition, diets containing 8% or 40% lipid were fed from lactation days 5-10 and mammary glands and livers of triplicate FVB mice prepared for microarray analysis. The results show that substantial regulation of lipid synthesis occurs at the level of mRNA expression and that some of the regulation points differ substantially from the liver. They also implicate the transcription factor SREBP-1c in regulation of part of the pathway.Physiological Genomics 03/2007; 28(3):323-36. · 2.81 Impact Factor